Critical role for the lung endothelial nonmuscle myosin light-chain kinase isoform in the severity of inflammatory murine lung injury.

ABSTRACT: Global knockout of the nonmuscle isoform of myosin light-chain kinase (nmMLCK), a primary cellular regulator of cytoskeletal machinery, is strongly protective in preclinical murine models of inflammatory lung injury. The current study was designed to assess the specific contribution of endothelial cell (EC) nmMLCK to the severity of murine inflammatory lung injury produced by lipopolysaccharide (LPS) and mechanical ventilation ventilator-induced lung injury or ventilation (VILI). Responses to combined LPS/VILI exposure were assessed in: (i) wild-type (WT) C57BL/6J mice; (ii) transgenic mice with global deletion of nmMLCK (nmMylk ^-/-); (iii) transgenic nmMylk ^-/- mice with overexpression of nmMLCK restricted to the endothelium (nmMylk ^-/-/ec-t

SUBMITTER: Kempf CL 

PROVIDER: S-EPMC9063969 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature